Key result
A single 4-hour inhalation exposure to diesel exhaust impaired cardiac performance and caused time-dependent oscillations in autonomic balance, including sympathetic dominance, in heart failure-prone rats.
Why the study?
Does diesel exhaust inhalation impair cardiac performance via autonomic nervous system imbalance in heart failure-prone rats?
Does diesel exhaust inhalation impair cardiac performance via autonomic nervous system imbalance in heart failure-prone rats?
Absolute Event Rate: 5425% vs 6489%
p-value: p=0.056
Acute inhalation of diesel exhaust causes time-dependent autonomic imbalance and decreases cardiac performance via aberrant sympathetic dominance in heart failure-prone rats.
No immediate change to heart failure management; leaves open translation of diesel exhaust autonomic effects from rat models to humans.
Cardiac disease exacerbation is associated with short-term exposure to vehicular emissions. Diesel exhaust (DE) might impair cardiac performance in part through perturbing efferent sympathetic and parasympathetic autonomic nervous system (ANS) input to the heart. We hypothesized that acute changes in ANS balance mediate decreased cardiac performance upon DE inhalation. Young adult heart failure-prone rats were implanted with radiotelemeters to measure heart rate (HR), HR variability (HRV), blood pressure (BP), core body temperature, and pre-ejection period (PEP, a contractility index). Animals pretreated with sympathetic antagonist (atenolol), parasympathetic antagonist (atropine), or saline were exposed to DE (500 µg/m(3) fine particulate matter, 4h) or filtered air and then treadmill exercise challenged. At 1 day postexposure, separate rats were catheterized for left ventricular pressure (LVP), contractility, and lusitropy and assessed for autonomic influence using the sympathoagonist dobutamine and surgical vagotomy. During DE exposure, atenolol inhibited increases in HR, BP, and contractility, but not body temperature, suggesting a role for sympathetic dominance. During treadmill recovery at 4h post-DE exposure, HR and HRV indicated parasympathetic dominance in saline- and atenolol-pretreated groups that atropine inhibited. Conversely, at treadmill recovery 21h post-DE exposure, HRV and PEP indicated sympathetic dominance and subsequently diminished contractility that only atenolol inhibited. LVP at 1 day postexposure indicated that DE impaired contractility and lusitropy while abolishing parasympathetic-regulated cardiac responses to dobutamine. This is the first evidence that air pollutant inhalation both causes time-dependent oscillations between sympathetic and parasympathetic dominance and decreases cardiac performance via aberrant sympathetic dominance.
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Carll et al. (2013) studied Heart failure-prone (n=49). Diesel exhaust vs. Filtered air was evaluated on Left ventricular contractility (dP/dtmax) 1 day post-exposure (p=0.056). A single 4-hour inhalation exposure to diesel exhaust impaired cardiac performance and caused time-dependent oscillations in autonomic balance, including sympathetic dominance, in heart failure-prone rats.
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